The present invention pertains to a cell culture medium comprising hypotaurine, GABA, and/or beta-alanine or the combination of choline and hypotaurine, GABA, and/or beta-alanine as media supplements which is shown to control viability, growth, and waste byproduct accumulation. The present invention further pertains to a method of producing a polypeptide of interest in a large scale cell culture containing hypotaurine, GABA, and/or beta-alanine or the combination of choline and hypotaurine, GABA, and/or beta-alanine.

The present invention pertains to a cell culture medium comprising hypotaurine, GABA, and/or beta-alanine or the combination of choline and hypotaurine, GABA, and/or beta-alanine as media supplements which is shown to control viability, growth, and waste byproduct accumulation. The present invention further pertains to a method of producing a polypeptide of interest in a large scale cell culture containing hypotaurine, GABA, and/or beta-alanine or the combination of choline and hypotaurine, GABA, and/or beta-alanine.

A TRAIL cell-penetrating peptide (CPPs)-like mutant MuR6 and a preparation method and the application thereof. The amino acid sequence of the mutant is SEQ ID NO: 2. The mutant selectively transforms the amino acid coding sequence of No. 114-119 of the outer fragment of the TRAIL wild-type protein cell membrane from VRERGP to RRRRRR, i.e., mutates valine into arginine on the 114.sup.th coding sequence, glutamic acid into arginine on the 116.sup.th coding sequence, glycine into arginine on the 118.sup.th coding sequence and proline into arginine on the 119.sup.th coding sequence, turning the coding sequence of N-terminal of the mutant protein into that of six arginines and making it a protein containing CPPs-like structure. Having a superior therapeutic effect on different types of tumor, the TRAIL mutant is a new generation of high-efficient drug for inducing tumor apoptosis of much potential.

A TRAIL cell-penetrating peptide (CPPs)-like mutant MuR6 and a preparation method and the application thereof. The amino acid sequence of the mutant is SEQ ID NO: 2. The mutant selectively transforms the amino acid coding sequence of No. 114-119 of the outer fragment of the TRAIL wild-type protein cell membrane from VRERGP to RRRRRR, i.e., mutates valine into arginine on the 114.sup.th coding sequence, glutamic acid into arginine on the 116.sup.th coding sequence, glycine into arginine on the 118.sup.th coding sequence and proline into arginine on the 119.sup.th coding sequence, turning the coding sequence of N-terminal of the mutant protein into that of six arginines and making it a protein containing CPPs-like structure. Having a superior therapeutic effect on different types of tumor, the TRAIL mutant is a new generation of high-efficient drug for inducing tumor apoptosis of much potential.

A TRAIL cell-penetrating peptide (CPPs)-like mutant MuR5 and a preparation method and the application thereof. The amino acid sequence of said mutant is SEQ ID NO: 2. The TRAIL CPPs-like mutant selectively transforms the amino acid coding sequence of No. 114-118 of the outer fragment of the TRAIL wild-type protein cell membrane from VRERG to RRRRR, i.e., mutates valine into arginine on the 114.sup.th coding sequence, glutamic acid into arginine on the 116.sup.th coding sequence and glycine into arginine on the 118.sup.th coding sequence, turning the coding sequence of N-terminal of the mutant protein into that of five arginines and making it a protein containing CPPs-like structure. Having a superior therapeutic effect on different types of tumor, the TRAIL CPPs-like mutant is a new generation of high-efficient drug for inducing tumor apoptosis of much potential.

BCMA-specific fibronectin type III (FN3) domains, BCMA-targeting chimeric antigen receptors (CARs) comprising the FN3 domains, and engineered BCMA-targeting immune cells expressing the CARs are described. Also described are nucleic acids and expression vectors encoding the FN3 domains and the CARs, recombinant cells containing the vectors, and compositions comprising the engineered immune cells. Methods of making the FN3 domains, CARs, and engineered immune cells, and methods of using the engineered immune cells to treat diseases including cancer are also described.

BCMA-specific fibronectin type III (FN3) domains, BCMA-targeting chimeric antigen receptors (CARs) comprising the FN3 domains, and engineered BCMA-targeting immune cells expressing the CARs are described. Also described are nucleic acids and expression vectors encoding the FN3 domains and the CARs, recombinant cells containing the vectors, and compositions comprising the engineered immune cells. Methods of making the FN3 domains, CARs, and engineered immune cells, and methods of using the engineered immune cells to treat diseases including cancer are also described.

The present invention relates, inter alia, to compositions and methods, including chimeric proteins having a first domain comprising an extracellular domain of a first transmembrane protein, a first secreted protein, or a first membrane-anchored extracellular protein and a second domain comprising an extracellular domain of a second transmembrane protein, a second secreted protein, or a second membrane-anchored extracellular protein, in which either or both of the first domain and the second domain decreases self-directed immune system activity when bound to its ligand/receptor. Accordingly, the present invention find use in the treatment of autoimmune diseases.

The present invention relates, inter alia, to compositions and methods, including chimeric proteins having a first domain comprising an extracellular domain of a first transmembrane protein, a first secreted protein, or a first membrane-anchored extracellular protein and a second domain comprising an extracellular domain of a second transmembrane protein, a second secreted protein, or a second membrane-anchored extracellular protein, in which either or both of the first domain and the second domain decreases self-directed immune system activity when bound to its ligand/receptor. Accordingly, the present invention find use in the treatment of autoimmune diseases.

Compositions specific for TNF-receptor superfamily member 25 (TNFRSF25, DR3) modulate the immune response by regulating T regulatory cells.